"The experiment was designed, therefore the results of the experiment were designed!" is a common IDiot response when faced with experimental results which nuke their assertions. It's also pretty stoopid, and you can make the stoopidity very obvious indeed with a few simple word-substitutions...

The roulette wheel was designed, therefore the sequence of numbers which come up on the wheel was designed!

The refrigerator was designed, therefore ice is designed!

Also, it's worth noting that the experiment was designed, therefore the results were designed is a veiled accusation of fraud on the part of scientists. It's saying that they got the results they got because they damn well made sure they got that particular set of results. Do your Creationist buddies really want to say that real scientists fabricate their experimental results?

They probably do, but they are too scared to. That opens them up for court action on libel.

--------------Ignored by those who can't provide evidence for their claims.

um, you do realize that Creationists accuse scientists of fraud and dishonesty on a regular basis, don't you?

But very rarely is it explicit or narrowed to one individual's attempt at any one thing. Most likely because the accusing creationists are pussies.... Creationists, I'd be happy to retract if proven wrong.

um, you do realize that Creationists accuse scientists of fraud and dishonesty on a regular basis, don't you?

AFAICT, Creationists tend not to explicitly, directly accuse scientists of fraud; the standard schtick (again, AFAICT) is to make some kind of statement or argument which is critically dependent on an unspoken presumption that scientists are frauds. Such as, just to pick a random example, the experiment is designed; therefore, the results are designed. It's not an explicit accusation of malfeasance, so it's not slander, right? Basically, it's the same old 'word magic' bullshit that Creationists indulge in so damn often. I suspect that most Creationists don't even realize what they're doing when they make veiled accusations of fraud/sleaze/turpitude... which is why it can be effective to drag such implicit accusations out into the cold, hard light of day where everybody can clearly see them for what they are.

um, you do realize that Creationists accuse scientists of fraud and dishonesty on a regular basis, don't you?

AFAICT, Creationists tend not to explicitly, directly accuse scientists of fraud; the standard schtick (again, AFAICT) is to make some kind of statement or argument which is critically dependent on an unspoken presumption that scientists are frauds. Such as, just to pick a random example, the experiment is designed; therefore, the results are designed. It's not an explicit accusation of malfeasance, so it's not slander, right? Basically, it's the same old 'word magic' bullshit that Creationists indulge in so damn often. I suspect that most Creationists don't even realize what they're doing when they make veiled accusations of fraud/sleaze/turpitude... which is why it can be effective to drag such implicit accusations out into the cold, hard light of day where everybody can clearly see them for what they are.

That's it...

and force them to actually conduct a dialogue about the paper they are trashing.

Fine, the experiment was designed. What part of the results were designed by the experimenters. Was the final RNA sequence designed? Was each mutation designed? etc. etc.

Hammer them on the science and on their non-answers.

Take everything they say to the next logical conclusion (as Cubist has shown with the roulette wheel).

"Oh, we weren't there so we don't know what happened? By that logic, unless the judge and jury were present at the crime, then no one could be convicted."

--------------Ignored by those who can't provide evidence for their claims.

Okay thank's for the imput everyone, but I ask you to be patient with me

I would really need my particular questions aswered. For the following reasons:

1) Some of the questions were placed by other readers of the forum and I'd like to answer them as they are pertinent questions.2) Some of the questions are my personal questions that help me with the better understanding.3) Some of the questions were placed directly at me by Ioseb

Yes of course I will finish with the conclusions that you have brought up and that should take care of the paper, but it's important to tie up the loose ends and give a more complete understanding.

Marty

--------------"Cows who know a moose when they see one will do infinitely better than a cow that pairs with a moose because they cannot see the difference either." Gary Gaulin

He is arguing that, the paper proves beyond doubt that there are hardly any gain of FCT mutations. So evolution can't occur. So it's all wrong.

Here are my accusations:

1) The paper is limited in that it only analises bacteria and viruses. No eukyrots are analised. So how the hell can you say that it applies to life in general.

I don't think this is a compelling argument on your part. First, the paper does include eukaryotes. All the mutations discussed in Table 1 are in human genes. Second, even if the paper does focus mostly on prokaryotes, they still comprise the longest extant lineage, dating back some 2 billion years, and a huge range of distinct functions first arose in prokaryotes. So if Behe's analysis really presented a fundamental problem for evolution, even just in prokaryotes, that would be a significant issue. Fortunately, his analysis does no such thing.

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2) The paper is limited to artificial experiments in which the process of natural selection has been removed. The only natural case examined was malaria.

I don't think this is a good criticism either. Even if most of the experiments involved selection in a lab environment, it's still a matter of some organism adapting to a new environment. The only real issue with lab-based studies, IMO, is that they're only able to assess evolution over periods of years to (at most) decades. They're not capable of directly observing the slow accretion of mutations and new functions that take place over thousands to billions of years. Naturally, the kinds of changes we see over ~ 10 years will look trivial compared to what can happen in 10 million years.

stating that: "The construction by mutation of a new promoter, intron/exon splice site, or protein processing site are gain-of-FCT mutations. Also included in this category is the divergence by mutation of the activity of a previously duplicated coded element.” In other words, mutations in this category produce new genes, parts of genes, or confer drastic new capabilities on genes by adding new splicing sites.

Also note that because almost no bacteria or viruses have introns in their cellular genes, it’s impossible to even see one class of this mutation in lab experiments on these groups.

a) What does this last paragraph mean? b) How does this relate to FCT gains?c) Is there evidence to support this?

Eukaryotes often have their protein coding sequences broken into separate bits called exons, with non-coding sequences called introns in between each exon. Bacteria don't usually do this - their protein coding sequences are typically uninterrupted. Some types of FCT gains involve rearrangement of introns and exons. Since bacteria don't usually have those, they can't generate that type of FCT gain.

All that said, I don't think this is a good criticism either. As noted above, bacteria have unquestionably developed new functions over evolutionary time. Really complicated structures like ribosomes, flagella, replication complexes, transporter proteins, etc., etc., all arose in prokaryotes first. So one way or another, bacteria must have developed novel functions over time.

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4) Behe states regarding Lenskies experiments: If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.

Do we have examples of gain-of-FCT mutations in experiments similar to Lenskies?

Behe's paper already lists some mutations that he classifyies as gain-of-FCTs. See Tables 2 & 4.

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5) Is there a specific reason that has arisen in other papers as to why most of the experiments lead to loss of FCT? I would answer that it is only due to the experimenters removing natural selection from the equation. Would I be right?

No, it's almost certainly because loss-of-FCT mutations are much more common than gain-of-FCT mutations. I can't readily offer a citation, but it's widely accepted that the vast majority of mutions in a protein coding sequence, for example, will either be neutral or deleterious to protein function. Only a few will enhance function or generate new functions (assuming we can agree on what a 'new function' really means). I don't think it's surprising that there will often be cases where a loss of FCT provides a selective advantage.

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6) The work is based on three organisms, prokaryotes, viruses and hemoglobin? Eukyrotes are not included in the study. Or does table 1 automatically include eukyrotes?

7) Plasmodium falciparum (malaria) is a eukyrote but the genetic mutation that is being studied is of Hemoglobin not of the malaria. Is this correct?

Hemoglobin and other genes in humans, yes.

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8) Isoeb makes the following case: The adaptation to Malaria is the sickle cell. Which is obviously due to FCT loss and leads to premature death. Only on extremely rare occasions do we get gain of FCT by Chloroquine Complexity Cluster or C Harlem. How rare is this gain let me tell you with C Harlem where the are two conections sites in the plasmid: it required 10^40 organisms to get this mutation. Seeing as there is only one known case.

Want to know how many organisims are estimated to have been around since start of life on the planet? 10^40.Do you know how may conection sites ther are in a cell 10.000.

Okay point one: I would say that he's making the stupid probability error again so I just fight this with the "evil killer dust bunny".Point two: What has this got to do with anything???

I have to guess with this one, because Ioseb is talking gibberish. I have no idea what "connection sites" are supposed to be, and plasmids have nothing to do with either chloroquine or malaria resistance.

A quick google of "C harlem" reveals that it's a particular hemoglobin variant where the B chain has two different amino acid substitutions. Most likely, Ioseb is trying to make the argument that it's nearly impossible for both of those mutations to have arisen simultaneously in one person, given the known mutation rate and the likely number of humans that have ever existed.

If so, there are two huge flaws in his argument. The first is his assumption that no other single or double mutations would have afforded malaria resistance. But in fact we know that's wrong, as Behe's own Table 1 shows. Thus, it's not a question of the probability of getting exactly those two mutations at some time during human evolution. It's a question of how many possible combinations of mutations would confer resistance, and whether it's reasonable that at least some of them could have arisen by chance during human evolution.

The other huge flaw is that Ioseb seems to be assuming that both mutations would have to arise at the same time in the same person. But that's obviously wrong. Nothing prevents one mutations from occurring and spreading through the population, before the second mutation occurs. And here's the kicker: it turns out that one of the two mutations in hemoglobin C harlem is the same mutation seen in conventional sickle cell disease. And we already know that lots of people have only that one mutation, and that that mutation alone confers malaria resistance. So it's easy to imagine that the sickle mutation happened first and spread to many individuals due to conferring resistance. The second mutation could have happened at some later date. Maybe the second mutation adds some additional selective advantage. (I didn't see anything about that either way in my brief search.) If so, that would be a perfect example of how evolution often works - incremental advantages adding on to previous ones.

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8) Ioseb calls my attenton to this site: www.ncbi.nlm.nih.gov/books/NBK7574/Saying that you see another study say exactly the same thing.

I looked at it and could find nothing of the sort...

Well, the first sentence of section 16.5.1 reads: "Making random changes in a gene is quite likely to stop it working, but very unlikely to give it a novel function." So Ioseb's point is probably again that gain-of-FCT mutations are uncommon. I already addressed this in my previous post: yes, but so what? Just because gain of function mutations are less common doesn't mean they don't happen (as even Behe acknowledges), and it doesn't mean they're too rare to support evolution. If Ioseb thinks they are too rare, he's going to need a lot more evidence than Behe's paper to make his case.

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9) My main argument is that okay so he saw loss of FCT functions in controlled environments in a few species of bacteria and virus (except the malaria) sooo what?

Exactly. Evolution clearly requires gain-of-FCT mutations, so if we never saw such mutations in lab studies, that might raise some questions. But we do see such mutations, so that's all fine. The fact that we see more loss-of-FCT mutations isn't a problem for evolution.

What he’s saying is this: “Yes, gain of FCTs could, and likely is, more important in nature than seen in these short-term experiments. But my conclusions are limited to these types of short-term lab studies.” Well, good, but then let us not hear Behe’s ID colleagues tout these results as giving strong conclusions about microbial or eukyaryotic evolution in nature, particularly because the lab studies deliberately exclude sources of gain-of-FCT mutations that we know are important in nature.

These “new genes,” then, would qualify as what Behe calls “gain-of-FCT” adaptive mutations (“FCT” = functional coded element): the kind of mutations that Behe did not see arising in short-term lab experiments on bacteria and viruses.

I was saying that, no matter what causes gain-of-FCT events to sporadically arise in nature (and I of course think the more complex ones likely resulted from deliberate intelligent design http://tinyurl.com/32n64xl....n64xl), short-term Darwinian evolution will be dominated by loss-of-FCT, which is itself an important, basic fact about the tempo of evolution.

Note the "likely resulted from ID" - the man has no idea whatsoever if they did or not, it's just "likely". Pathetic is as pathetic does.

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Any mutation which confers an advantage at any time will be selected, and the large majority of those in the short term will be LOF.

A "large majority" again. So even Behe admits that evolution can "create" as well as "destroy".

--------------I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot standGordon Mullings

Just a consideration, is it possible that oraganisms left to themselves, without the pressures of natural competative selection would automatically tend toward loss of function.

After all they would just be responding to the new situation which requires less complex machinery.

I don't think there is, or even can be, an environment "without the pressures of natural competative selection".Let's suppose an species is 'perfectly' adapted to its environment (for whatever value of 'perfectly'), and let's further suppose that its environment is stable over geologically relevant periods of time. Even in such a situation, there's going to be a finite quantity of resources available at any one time, and members of the species will be competing against each other for those resources. Voila -- natural selection! As well, mutations will occur, and some of those mutations will render their possessors more or less able to produce offspring, as compared to their fellow critters who lack the reproduction-affecting mutations. Again, natural selection.In short: You can't get rid of competition, because if nothing else, critters compete against each other.

Just a consideration, is it possible that oraganisms left to themselves, without the pressures of natural competative selection would automatically tend toward loss of function.

After all they would just be responding to the new situation which requires less complex machinery.

What are your thoughts on this?

ThanksMarty

Well, like others have said, you can never completely escape from selection. Even if all resources were infinite, there would still be selection against mutations that cause death or infertility.

That said, there are lots of examples where organisms have lost functions that were no longer essential. A very well known example is that humans and related primates have lost the ability to synthesize vitamin C.

In some cases, there may even be advantages to not making something that's no longer needed.

(snip)"Making random changes in a gene is quite likely to stop it working, but very unlikely to give it a novel function." So Ioseb's point is probably again that gain-of-FCT mutations are uncommon. I already addressed this in my previous post: yes, but so what? Just because gain of function mutations are less common doesn't mean they don't happen (as even Behe acknowledges), and it doesn't mean they're too rare to support evolution. If Ioseb thinks they are too rare, he's going to need a lot more evidence than Behe's paper to make his case.

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9) My main argument is that okay so he saw loss of FCT functions in controlled environments in a few species of bacteria and virus (except the malaria) sooo what?

Exactly. Evolution clearly requires gain-of-FCT mutations, so if we never saw such mutations in lab studies, that might raise some questions. But we do see such mutations, so that's all fine. The fact that we see more loss-of-FCT mutations isn't a problem for evolution.

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Thanks for your imput on this

Marty

You're welcome. I hope that's helpful.

Creationists have this strawman / misunderstanding / deliberate misrepresentation of life / evolution / Creation as a constant forward march to perfection, i.e., us.

They forget or ignore that 99% of all species that ever existed are now extinct. We are the 1%! :-)

So the rarity of beneficial mutations comes as no surprise to anyone, really.

Forget "survival of the fittest", evolution is just "reproduction of the fit enough", aka live long enough to get laid.

eta "mis"

--------------"But it's disturbing to think someone actually thinks creationism -- having put it's hand on the hot stove every day for the last 400 years -- will get a different result tomorrow." -- midwifetoad

[quote=Southstar,Dec. 02 2011,13:22][/quote]New chew toy people, since Ioseb has found this forum, I've asked him if he would like to come here a debate with you directly. He has some "fascinating" ideas about Behe and co.

I challenged him to come here and debate with you guys. Hopefully he'll say yes. I really hope he does...

let see..

Marty

He's too chicken. Only the truly brain dead will come here and argue for more than a few posts.

You ought to read the AFDave threads. There's also another one for FT. Good reads.

--------------Ignored by those who can't provide evidence for their claims.

“Our data shows that evolution of novel structures can occur on extremely short time scales. Cecal valve evolution probably went hand-in-hand with a novel association between the lizards on Pod Mrcaru and microorganisms called nematodes that break down cellulose, which were found in their hindguts.”

--------------I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot standGordon Mullings

How would gain of function derive from speciation? Speciation just means that some subset of the species is now evolving separately from the rest of it. Seems to me that that's independent of whether either part of the population had a gain of function or not.

I've been looking for some example of gain-of-function mutation that has derived from speciation.

That seems backwards to me. Mutations, including gain-of-function mutations in specific, are the stuff of which speciation is made, not so? Wouldn't it be more reasonable to ask for examples of speciation derived from gain-of-function mutation, rather than the other way around?

I've been looking for some example of gain-of-function mutation that has derived from speciation.

That seems backwards to me. Mutations, including gain-of-function mutations in specific, are the stuff of which speciation is made, not so? Wouldn't it be more reasonable to ask for examples of speciation derived from gain-of-function mutation, rather than the other way around?

Most speciation is not driven by natural selection, but by accumulation of genetic differences. Lenski's E coli experiment showed a gain of function - ability to use citrate as a nutrient.

--------------"Following what I just wrote about fitness, you’re taking refuge in what we see in the world." PaV

“Our data shows that evolution of novel structures can occur on extremely short time scales. Cecal valve evolution probably went hand-in-hand with a novel association between the lizards on Pod Mrcaru and microorganisms called nematodes that break down cellulose, which were found in their hindguts.”

Hi,

The objection made to this article is that there is no proof of novel genetic material in the study. Actually in all fairness it does state "Tail clips taken for DNA analysis confirmed that the Pod Mrcaru lizards were genetically identical to the source population on Pod Kopiste."

So one could assume that the mutations are only induced by the enviroment and are not genetic based?

another thing I have replied to this saying that the development of the Cecal valve which is only been developed on the lizards of one island can only be produced with an increase of the amount of genetic material. Would this be correct?

Or would it be possible that these genes were somehow latent and were only expressed when the animal turned to a heavier herbivourous diet?

ThanksMarty

--------------"Cows who know a moose when they see one will do infinitely better than a cow that pairs with a moose because they cannot see the difference either." Gary Gaulin

“Our data shows that evolution of novel structures can occur on extremely short time scales. Cecal valve evolution probably went hand-in-hand with a novel association between the lizards on Pod Mrcaru and microorganisms called nematodes that break down cellulose, which were found in their hindguts.”

Hi,

The objection made to this article is that there is no proof of novel genetic material in the study. Actually in all fairness it does state "Tail clips taken for DNA analysis confirmed that the Pod Mrcaru lizards were genetically identical to the source population on Pod Kopiste."

So one could assume that the mutations are only induced by the enviroment and are not genetic based?

another thing I have replied to this saying that the development of the Cecal valve which is only been developed on the lizards of one island can only be produced with an increase of the amount of genetic material. Would this be correct?

Or would it be possible that these genes were somehow latent and were only expressed when the animal turned to a heavier herbivourous diet?

ThanksMarty

There is proof in Lenski's experiment.

--------------"Following what I just wrote about fitness, you’re taking refuge in what we see in the world." PaV